Abstract
In the isolated perfused rat kidney renin release is increased by physiological agents which stimulate adenylate cyclase activity, such as beta-adrenoceptor agonists, prostaglandins, histamine (histamine H2-receptor mediated) and adenosine (adenosine RA-receptor mediated). The role of adenylate cyclase and cAMP in the stimulatory pathway for renin release was confirmed by the effect of forskolin, a receptor-independent stimulator of adenylate cyclase, which also stimulated renin release. The intracellular calmodulin-calcium complex was identified as part of an opposing inhibitory pathway. This conclusion is based on the observation that various inhibitors of calmodulin stimulated renin release and that the calcium-dependent inhibition of renin release by angiotensin II was abolished in the presence of these inhibitors. The intracellular control mechanisms for renin release are discussed with respect to the vascular smooth muscle origin of renin-producing cells.
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